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Herrera, Añazco Percy, Holguín Edward Mezones i Adrian V. Hernández. "Global kidney disease". Elsevier B.V, 2014. http://hdl.handle.net/10757/322401.
Pełny tekst źródłaRevisión por pares
Wei, Jin. "Acute Kidney Injury and Chronic Kidney Disease". Scholar Commons, 2017. http://scholarcommons.usf.edu/etd/6780.
Pełny tekst źródłaPhilips, L. G. "Disease management in chronic kidney disease /". abstract and full text PDF (free order & download UNR users only), 2005. http://0-wwwlib.umi.com.innopac.library.unr.edu/dissertations/fullcit/1430446.
Pełny tekst źródła"May, 2005." Includes bibliographical references (leaves 92-97). Online version available on the World Wide Web. Library also has microfilm. Ann Arbor, Mich. : ProQuest Information and Learning Company, [2005]. 1 microfilm reel ; 35 mm.
Papadopoulos, Theofilos. "MiRNAs in kidney disease". Thesis, Toulouse 3, 2016. http://www.theses.fr/2016TOU30194/document.
Pełny tekst źródłaMicroRNAs are now recognized as key players in the regulation of proteins and any abnormality in their function is a cause for pathway instability, leading to pathological conditions. Numerous reports from a variety of pathologies provide new data about microRNAs function, their targets and their potential as biomarkers and possible ways to control microRNAs' expression for potential therapeutic purpose. A number of reports also connect microRNAs with pathological conditions in the kidney and point to the use of microRNAs as biomarkers for diagnosis and prognosis of kidney disease in blood, serum, tissue and urine samples. In this thesis, we researched:1) A possible role of the microRNAs in the progression of adult chronic kidney disease (CKD), a disease representing a global burden with the tendency to rise worldwide. Progression of CKD is still very hard to detect non-invasively with the currently used clinical tools (eGFR and albuminuria). In our work we studied alterations of the level of the microRNAs in human urine samples of patients with fast or slow progression of CKD, in order to identify new potential biomarkers for non-invasive progression of CKD. Using Next Generation Sequencing, we analyzed urinary microRNA modifications in urine samples of 70 patients with established CKD and correlated their expression profiles to disease progression. This lead to the identification of 25 urinary microRNAs significantly associated to CKD progression (adjusted pvalue<0.05). Among those, four microRNAs (hsa-miR-34c-5p, hsa-miR-410-3p, hsa-miR-301b-3p, and hsa-miR-145-5p) were selected for validation in an independent cohort of 52 patients with CKD. Increased urinary abundance of hsa-miR-145-5p was confirmed to be associated to progression of CKD. In vitro exploration of the effects of hsa-miR-145-5p inhibition in human kidney cells showed that the microRNA seemed to be involved in necrotic processes. In conclusion we have identified hsa-miR-145-5p as potential urinary microRNA marker of CKD progression. 2) The identification of microRNAs associated to obstructive nephropathy, a frequently encountered disease in children that can lead, in severe cases, to end stage renal disease (ESRD). In this study we used a comprehensive system biology analysis in which we combined micro- and mRNA data from human and animal obstructive nephropathy to obtain information on possible mechanisms involved in this disease. In particular, we have studied in parallel the urinary miRNome of infants with ureteropelvic junction (UPJ) obstruction and the kidney tissue miRNome and transcriptome of the corresponding neonatal partial unilateral ureteral obstruction (UUO) mouse model. Several hundreds of microRNAs and mRNAs displayed changed abundance during disease. Combination of microRNAs in both species and associated mRNAs let to the prioritization of 5 microRNAs and 35 mRNAs associated to disease. In vitro and in vivo validation identified consistent dysregulation of let-7a-5p and miR-29-3p and new potential targets, E3 ubiquitin-protein ligase (DTX4) and neuron navigator 1 (NAV1). Our study is the first to correlate a mouse model of neonatal partial UUO with human UPJ obstruction in a comprehensive systems biology analysis. Our data revealed let-7a and miR-29b as molecules potentially involved in the development of fibrosis in UPJ obstruction via the control of DTX4 in both man and mice that would not be identified otherwise
Ramzan, Naveen, Shimin Zheng, Hemang Panchal, Edward Leinaar, Christian Nwabueze i Timir K. Paul. "Investigating The Association Between Chronic Kidney Disease and Clinical Outcomes". Digital Commons @ East Tennessee State University, 2019. https://dc.etsu.edu/asrf/2019/schedule/21.
Pełny tekst źródłaGale, D. "Genetic investigation of kidney disease". Thesis, University College London (University of London), 2010. http://discovery.ucl.ac.uk/763753/.
Pełny tekst źródłaWong, Germaine. "Cancer and chronic kidney disease". Thesis, The University of Sydney, 2008. https://hdl.handle.net/2123/28229.
Pełny tekst źródłaBrunmark, Charlott. "Type IV collagen and renal disease". Lund : Dept. of Nephrology, University of Lund, 1994. http://books.google.com/books?id=owdrAAAAMAAJ.
Pełny tekst źródłaAntoniv, A. A. "Kidneys functional status in patients with chronic kidney disease and nonalcoholic steatohepatitis". Thesis, БДМУ, 2020. http://dspace.bsmu.edu.ua:8080/xmlui/handle/123456789/18082.
Pełny tekst źródłaPatenaude, Anne-Marie. "Wnt signaling in kidney development and implication in polycystic kidney disease". Thesis, McGill University, 2005. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=84066.
Pełny tekst źródłaThere is also evidence that non-canonical Writ signaling may be involved in the development of renal cysts but this pathway is uncharacterized. We therefore studied the ontogeny of a downstream marker of this pathway (NFAT) and its localization in the developing kidney. Here we report that NFAT activity is high in early stages of kidney development and is rapidly downregulated at birth. The NFAT signal is diffuse and is expressed in both mesenchymal and epithelial cells of the developing kidney.
Miller, Michelle. "WNT signalling in kidney development and autosomal dominant polycystic kidney disease". Thesis, McGill University, 2011. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=103736.
Pełny tekst źródłaLors du développement rénal, il y a une permutation entre les voies canonique et non-canonique de signalisation WNT. Ce changement permet au rein en développement de passer d'un état de prolifération active à une différentiation terminale. La pensée actuelle est qu'une erreur lors de cette transition est un mécanisme sous-jacent dans la pathologie de la maladie polykystique autosomale dominante des reins. Nous avons tout d'abord émis l'hypothèse que manquer de réprimer la voie canonique de signalisation WNT conduirait à la formation de kyste. En suivant ce raisonnement, nous avons croisé des animaux disposant d'un gène rapporteur de l'activité transcriptionnelle de -caténine à ceux présentant des mutations dans Pkd1 ou Pkd2. Nous n'avons trouvé aucune signalisation aberrante de la voie canonique de WNT dans les cellules épithéliale tapissant les kystes et en avons conclu qu'un échec de restriction de l'activité transcriptionnelle de -caténine n'est pas la cause de la maladie polykystique autosomale dominante des reins. Nous avons ensuite examiné si une incapacité d'activer une voie non-canonique de signalisation WNT, plus précisément la voie WNT-calcium, contribue à la formation de kyste. La voie WNT-calcium n'a pas été caractérisée au préalable dans le rein en développement. Nous avons donc établi des cultures cellulaires, d'organe et des systèmes in vitro afin d'étudier la voie de signalisation dans un contexte développemental normal. Nous avons alors montré que l'activité de la voie de signalisation culmine au jour embryonnaire (E)13 à E16 et se localise dans la zone néphrogénique des reins E16. De plus, nous avons démontré que l'activation de la voie WNT-calcium in vitro réduit la motilité des cellules, un processus important lors de la condensation des cellules mésenchymateuses pour former la vésicule rénale. Afin d'évaluer le rôle de la voie de signalisation WNT-calcium dans la maladie polykystique autosomale dominante des reins, nous avons croisé des souris disposant d'un gène rapporteur de l'activité transcriptionnelle de NFAT à celles présentant une mutation dans Pkd2. Nous avons constaté que l'activité de la voie de signalisation est considérablement réduite dans les reins kystiques. Ensemble, cette étude confirme l'hypothèse selon laquelle il y aurait une permutation développementale entre les voies canonique et non-canonique de signalisation WNT durant le développement normal du rein, et suggère que l'absence de toute activité de la voie WNT-calcium pourrait être un facteur contribuant à la pathogenèse de la maladie polykystique autosomale dominante des reins.
Yengkopiong, Jada. "Characterization of polycystic kidney disease in the Lewis Polycystic Kidney rat". Thesis, Yengkopiong, Jada (2010) Characterization of polycystic kidney disease in the Lewis Polycystic Kidney rat. PhD thesis, Murdoch University, 2010. https://researchrepository.murdoch.edu.au/id/eprint/4067/.
Pełny tekst źródłaTomlinson, Laurie. "Arterial Stiffness and Chronic Kidney Disease". Thesis, University of Brighton, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.518323.
Pełny tekst źródłaLi, Zhaoli Amy, i 李昭立. "Aquaporins in kidney development and disease". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2004. http://hub.hku.hk/bib/B29505987.
Pełny tekst źródłaConnor, T. M. F. "A study of inherited kidney disease". Thesis, University College London (University of London), 2013. http://discovery.ucl.ac.uk/1398923/.
Pełny tekst źródłaNavaneethan, Sankar. "METABOLIC SYNDROME AND CHRONIC KIDNEY DISEASE". Case Western Reserve University School of Graduate Studies / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=case1401967446.
Pełny tekst źródłaXie, Jeffrey Xinshuo. "Molecular Insights into Chronic Kidney Disease". University of Toledo Health Science Campus / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=mco1500201100900825.
Pełny tekst źródłaWhite, Joanna D. "Investigations into feline chronic kidney disease". Thesis, The University of Sydney, 2010. https://hdl.handle.net/2123/28931.
Pełny tekst źródłaSo, Beng Hock. "Chronic kidney disease : determining chronicity, prevalence, variation and survival in a community chronic kidney disease (CKD) cohort". Thesis, University of Glasgow, 2018. http://theses.gla.ac.uk/30671/.
Pełny tekst źródłaClark, Laura Elizabeth. "The epidemiology of chronic kidney disease in Grampian". Thesis, Available from the University of Aberdeen Library and Historic Collections Digital Resources, 2009. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?application=DIGITOOL-3&owner=resourcediscovery&custom_att_2=simple_viewer&pid=33407.
Pełny tekst źródłaO’Lone, Emma. "Cardiovascular disease: priorities and outcomes in end stage kidney disease". Thesis, The University of Sydney, 2020. https://hdl.handle.net/2123/22326.
Pełny tekst źródłaWarner, Joshua Dale. "Kidney segmentat ion and image analysis in autosomal dominant polycystic kidney disease". Thesis, College of Medicine - Mayo Clinic, 2016. http://pqdtopen.proquest.com/#viewpdf?dispub=10111486.
Pełny tekst źródłaAutosomal Dominant Polycystic Kidney Disease (ADPKD) is among the most prevalent life-threatening genetic conditions. Despite this, no approved medical therapies exist to treat the disease. Until the recent past, no methods could reliably measure the course of the disease far in advance of end stage renal disease (ESRD). As normal tissue is progressively destroyed or blocked by enlarging cysts, remaining nephrons compensate in a process called hyperfiltration. This beneficial physiological response confounds tests of renal function. Thus, potential interventions could not be tested against a reliable measurement of disease progression.
However, progressive changes are visually apparent on medical imaging examinations throughout the course of ADPKD. The search for ADPKD proxy biomarkers is now focused on quantitative imaging, or the extraction of information from medical images for purposes of diagnosis or disease tracking. Recent studies from the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)- sponsored Consortium for Radiologic Imaging Studies of Polycystic Kidney Disease (CRISP) showed Total Kidney Volume (TKV) is a usable quantitative imaging biomarker which can track disease in the early, asymptomatic phase and register measurable changes in as little as 12 months. These findings launched several new trials into potential ADPKD therapies.
Advanced analysis of polycystic kidney images, however, has never been done. The method CRISP used to extract TKV was stereology, an efficient means to estimate volume. However, stereology was tradi- tionally a dead end for further advanced analysis. TKV is useful for clinical trials and large population-based studies, but cannot accurately predict disease progression or stratify risk due to known out- lier cases. Thus, the utility of TKV for individual patient prognosis is limited. This work builds upon stereology data, describing a reliable and accurate new semi-automatic method to fully segment images us- ing only labeled stereology grids. Then, two new second generation quantitative imaging biomarkers are introduced and analyzed: Cyst- Parenchyma Surface Area (CPSA) and cyst concentration. These new physiologically motivated biomarkers will complement or potentially replace TKV in efforts to bring quantitative imaging to individual patients.
The goal of this body of work is to enable a pathway for efficient advanced image analysis in ADPKD, never before attempted in this dis- order, and to define new quantitative imaging biomarkers which will complement or replace existing ones in hopes of making individualized disease tracking for ADPKD patients a reality.
Müller, Tilman [Verfasser]. "Apelinergic system in the kidney: implications for diabetic kidney disease / Tilman Müller". Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2020. http://d-nb.info/1218075961/34.
Pełny tekst źródłaAntoniv, A. A. "The kidneys functional state in chronic kidney disease in patients with nonalcoholic steatohepatitis". Thesis, БДМУ, 2021. http://dspace.bsmu.edu.ua:8080/xmlui/handle/123456789/18584.
Pełny tekst źródłaHermans, Marcus Matheus Hendrik. "Arterial wall abnormalities in chronic kidney disease". Maastricht : Maastricht : Universitaire Pers Maastricht ; University Library, Universiteit Maastricht [host], 2007. http://arno.unimaas.nl/show.cgi?fid=9384.
Pełny tekst źródłaParham, Rhian. "Caregiver burden in paediatric chronic kidney disease". Thesis, Canterbury Christ Church University, 2011. http://create.canterbury.ac.uk/10347/.
Pełny tekst źródłaHuang, J. L. "Polycystic kidney disease and the renal circulation". Thesis, University College London (University of London), 2013. http://discovery.ucl.ac.uk/1416827/.
Pełny tekst źródłaZhou, Yu Simona. "Podocyte repair and recovery in kidney disease". Thesis, University of Edinburgh, 2011. http://hdl.handle.net/1842/5959.
Pełny tekst źródłaVerdeguer, Francisco. "Role of HNF1β in Polycystic Kidney Disease". Paris 6, 2010. http://www.theses.fr/2010PA066543.
Pełny tekst źródłaFerreira, Luciana Carolina Lopes. "Autosomal dominant polycystic kidney disease - genetic diagnosis". Master's thesis, Universidade de Aveiro, 2012. http://hdl.handle.net/10773/10731.
Pełny tekst źródłaA doença renal poliquística autossómica dominante (ADPKD) é uma doença hereditária e monogénica comum que resulta no desenvolvimento de quistos renais que aumentam em tamanho e em número com o avanço da idade, muitas vezes conduzindo ao aparecimento da doença renal terminal. Cerca de 85% dos casos identificados são causados por mutações no gene PKD1, um gene complexo de elevadas dimensões (~ 47kb). Atualmente, a sequenciação completa do gene PKD1 permite, com elevada sensibilidade, detetar variantes alélicas e pode ser utilizada em determinadas situações clínicas para as quais as técnicas radiológicas não permitem obter um diagnóstico clínico definitivo. No entanto, o rastreio de mutações é muitas vezes inconclusivo devido à presença de várias cópias homólogas a este gene localizadas no cromossoma 16, e à elevada heterogeneidade alélica do PKD1. O presente trabalho teve como objetivo o desenvolvimento de um teste genético de diagnóstico para a ADPKD através da sequenciação da zona codificante e limites intrão/exão do gene PKD1, utilizando a tecnologia de Sanger e otimizado para amostras de sangue armazenadas em cartões FTA™. Procedeu-se à otimização da amplificação e sequenciação, das regiões de interesse, utilizando a tecnologia de BigDye™ Terminator V3.1 e o protocolo desenvolvido mostrou ser uma metodologia reprodutível. Mutações patogénicas foram rastreadas em amostras de dois indivíduos, não relacionados, com ADPKD. Num dos pacientes a análise revelou a presença de uma mutação causadora de um codão stop prematuro no exão 15, no segundo paciente foi detetada uma deleção de 19pb no intrão 31, originando uma alteração na frame de leitura e causando a terminação prematura da proteína. Além disso, a heterogeneidade do PKD1 foi verificada uma vez que foram detetadas várias variantes neutras nas amostras analisadas, sendo que três destas alterações resultaram em alteração de aminoácido. Este estudo demonstrou o potencial da sequenciação de Sanger no diagnóstico de doenças genéticas. Apesar de futuramente ser necessária a validação com mais amostras de pacientes com ADPKD, é possível concluir que a metodologia desenvolvida poderá conduzir a um diagnóstico genético eficaz.
Autosomal Dominant Polycystic Kidney Disease (ADPKD) is a common hereditary and monogenic disorder that results in renal cysts development that increases in number and size as the person gets older, often leading to end- stage renal disease. PKD1 is a large (~47kb) and complex gene that accounts for 85% of the identified cases of ADPKD. Currently, the full sequencing of PKD1 allows, with high sensibility, the detection of variations along the gene and this may be used in certain clinicai situations where imaging cannot provide a definitive clinicai diagnosis. However, the screening of mutation is often inconclusive because of multiple homologous copies of this gene on chromosome 16 and the high levei of allelic heterogeneity of PKD1. The research presented here had the objective to develop a genetic diagnostic test for ADPKD through PKD1 coding region and exon/intron boundaries sequencing, using Sanger technology and optimized for blood samples in FTA™ cards. The amplification and sequencing, using BigDye™ Terminator V3.1 technology, were optimized for the regions of interest, and the methodology showed to be reproducible. The screening for disease-causing mutations was performed in two unrelated individuais with ADPKD. The analysis revealed the presence of a truncating mutation in exon 15 in one of the patients, and a 19bp deletion in intron 31 of the other patient, which led to frameshifting and premature termination. In addition, the heterogeneity of PKD1 was observed, since there were detected several neutral variants in the analyzed samples, three of which resulting in amino acid substitution. This research demonstrated the potential of automated Sanger sequencing for diagnosis of genetic diseases. Although further validation using more samples from ADPKD patients is still needed, it is possible to conclude that this approach can lead to an effective molecular genetic diagnosis.
Manfredi, Eugene Trent. "Immunodiagnostic methods for the detection of bacterial kidney disease in salmonid fishes /". Thesis, Connect to this title online; UW restricted, 1986. http://hdl.handle.net/1773/5282.
Pełny tekst źródłaGallagher, Sean. "Reducing acute kidney injury in patients with chronic kidney disease undergoing cardiac surgery". Thesis, Queen Mary, University of London, 2014. http://qmro.qmul.ac.uk/xmlui/handle/123456789/8669.
Pełny tekst źródłaScholes-Robertson, Nicole. "Improving access to kidney replacement therapy for rural Australians with chronic kidney disease". Thesis, The University of Sydney, 2022. https://hdl.handle.net/2123/28686.
Pełny tekst źródłaBrizi, Valerio. "Engineering complex kidney structures for disease modelling, drug testing, and studying kidney development". Thesis, Open University, 2018. http://oro.open.ac.uk/53445/.
Pełny tekst źródłaYau, Chung-fai Forrest. "DNA microsatellites co-segregation of polycystic kidney disease genes (PKD1 & PKD2) in autosomal dominant polycystic kidney disease (ADPKD) families & cell culture models for ADPKD /". Hong Kong : University of Hong Kong, 1999. http://sunzi.lib.hku.hk/hkuto/record.jsp?B21904030.
Pełny tekst źródłaUniacke, Mark. "The natural history of acute kidney injury and its relationship to chronic kidney disease". Thesis, University of Southampton, 2012. https://eprints.soton.ac.uk/361330/.
Pełny tekst źródłaChitalia, Nihil A. "Vitamin D, inflammation and cardiovascular disease in patients with chronic kidney disease". Thesis, St George's, University of London, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.616978.
Pełny tekst źródłaKim, Siah. "Chronic kidney disease and cardiovascular disease in Aboriginal children and young adults". Thesis, The University of Sydney, 2016. http://hdl.handle.net/2123/15945.
Pełny tekst źródłaPalanca, Ana. "Subclinical atherosclerosis in chronic kidney disease and diabetes". Doctoral thesis, Universitat Autònoma de Barcelona, 2020. http://hdl.handle.net/10803/670707.
Pełny tekst źródłaLa enfermedad cardiovascular es la primera causa de morbilidad y mortalidad mundial. Los individuos con diabetes y enfermedad renal crónica (ERC) presentan un mayor riesgo de eventos cardiovasculares (ECV) con respecto a la población general. En la diabetes, el incremento del riesgo cardiovascular es heterogéneo y se ha relacionado con el grado de afectación renal. Por otra parte, los algoritmos tradicionales para calcular el riesgo cardiovascular no trasladan con suficiente precisión el riesgo futuro de ECV. La evaluación de la aterosclerosis subclínica (AS) mediante ecografía multiterritorial representa una herramienta válida para refinar el riesgo cardiovascular. El propósito de esta tesis fue analizar mediante ecografía multiterritorial la prevalencia, distribución y progresión de AS, así como factores de riesgo asociados, en una amplia cohorte de pacientes, sin enfermedad cardiovascular, con ERC y con y sin diabetes. Posteriormente, se evaluó el valor pronóstico de la AS para determinar la incidencia de ECV en esta población de alto riesgo. Inicialmente, se analizaron los datos de los sujetos con ERC, con diabetes y sin diabetes, de la cohorte del estudio NEFRONA reclutados al inicio del estudio y que asistieron a la visita de control a los 24 meses. Tras realizar un estudio ultrasonográfico carotídeo y femoral tanto en la visita inicial como en la de seguimiento, se evaluó la correlación de factores de riesgo asociados con prevalencia y progresión de placa mediante análisis multivariables. Asimismo, se realizó otro análisis con todos los sujetos del NEFRONA, con y sin diabetes, reclutados inicialmente y a los que se les siguió durante 48 meses. Durante el periodo de seguimiento se registraron los ECV incidentes. Se utilizaron análisis bivariados y análisis de modelo de riesgos competitivos de Fine-Grey para el estudio estadístico. El índice C se estimó para los modelos de riesgo resultantes con mayor potencia. Como resultados, se observó que la proporción de individuos con placa basal fue mayor entre los sujetos con diabetes. Los sujetos con diabetes presentaron con mayor frecuencia la afectación con placa de más de dos territorios vasculares. También se observó una mayor progresión de placa en los individuos con diabetes. Tras realizar el análisis multivariable, se demostró que la presencia de placa basal se asociaba con la edad, el género masculino, el hábito tabáquico y la diálisis en los sujetos sin diabetes mientras que, en los sujetos con diabetes, la presencia de placa basal se asoció tan sólo a la edad y al género masculino. La progresión de placa se asoció a la edad, al número de territorios con placa basal, al hábito tabáquico y a la diálisis en ambos grupos. Se registraron 107 ECV entre los sujetos sin diabetes (19.58 por 1000 años-persona) y 96 entre los sujetos con diabetes (44.44 por 1000 años-persona). El modelo que mejor predijo futuros ECV en individuos sin diabetes contenía las variables: edad, 25-OH vitamina D y número de territorios con placa basal. Entre los participantes con diabetes el modelo más robusto en predecir ECV incidentes contenía tan sólo la variable ‘número de territorios con placa basal’. Para ambos modelos, el índice estadístico C, estimado a los 24 y a los 48 meses, fue superior a 0.70. La AS es más prevalente, conlleva mayor carga y es más progresiva en individuos con ERC y diabetes. En estos sujetos, la diabetes supera otros factores de riesgo descritos. Así mismo, la carga de AS es el predictor más potente de futuros ECV en individuos con diabetes y ERC. La detección precoz de carga AS mediante ultrasonografía multiterritorial podría mejorar la predicción de ECV en esta población.
Cardiovascular disease (CVD) is the leading cause of morbidity and mortality worldwide. Individuals with diabetes and chronic kidney disease (CKD) have remarkably high rates of CVD risk. Moreover, incremental cardiovascular risk in diabetes is heterogeneous and has been often related to concomitant CKD. Typically used risk equations based on traditional cardiovascular risk factors fail to accurately predict cardiovascular risk not only in the general population but also in these subsets of the population. Multi-territorial ultrasonography to assess subclinical atherosclerosis (SA) has emerged as a valid tool to refine cardiovascular risk assessment beyond traditional risk factors. The purpose of this thesis was to analyse the prevalence, distribution, and progression of SA, as well as the associated cardiovascular risk factors in a large cohort of CKD subjects with and without diabetes, free from CVD, using multi-territorial ultrasonography. Subsequently, we further evaluated the prognostic value of SA in determining the incidence of first cardiovascular events (CVE) in this high-risk population. First, we included the data from CKD subjects with and without diabetes and free from previous CVE from the NEFRONA cohort, that were recruited at baseline, and that attended a follow-up visit 24 months later. Participants underwent carotid and femoral ultrasound examinations at baseline and at 24-month follow-up. Risk factors associated with the prevalence and progression of SA were evaluated using multivariate model analyses. In the second hand, we also conducted another analysis including data from the NEFRONA cohort subjects with and without diabetes that were recruited initially and were followed-up for 48 months. During the follow-up period, all CVE were registered. Bivariate analysis and Fine-Gray competing risk models were used to perform the statistical analysis. Concordance Index (C-statistics) was estimated for the strongest resulting risk models. We found that at baseline, the proportion of subjects with plaque at any of the examined territories was higher among diabetic individuals. Diabetic subjects more frequently had more than two vascular territories with plaque. During a 24-month follow-up period, plaque progression occurred in 72.2% individuals with diabetes whereas, among individuals without diabetes, plaque progression occurred in 55.8%. Multivariable analysis indicated that plaque at baseline was significantly associated with age, male gender, smoking, and dialysis in the non-diabetic subjects, while only age and male gender were associated with plaque presence in diabetic subjects. Plaque progression was significantly associated with age, the number of territories with basal plaque, smoking, and renal replacement therapy in both groups. Additionally, during a mean follow-up time of 48 months, CVE rate among participants without diabetes was 19.58 per 1000 person-years and 44.44 per 1000 person-years among participants with diabetes. After competing risk analyses and model selection, those variables that better predicted CVE in individuals without diabetes were the number of territories with plaque, age and serum concentrations of 25-OH vitamin D. Among participants with diabetes, the strongest model predicting incident CVE had only one variable: the number of territories with basal plaque. For both models, the concordance (C) index score was greater than 0.7 at both 24 and 48 months. We concluded that SA is more prevalent, carries a higher plaque burden, and is more progressive in CKD subjects with diabetes than in CKD subjects without diabetes. In these individuals, diabetes outweighs other risk factors associated with the presence of SA. SA is the strongest predictor of future CVE in diabetic individuals with CKD. Early detection of the SA burden by multi-territorial vascular ultrasound could improve CVE prediction in this population.
Webster, Angela C. "Immunosuppression and malignancy in end stage kidney disease". Connect to full text, 2006. http://hdl.handle.net/2123/1186.
Pełny tekst źródłaTitle from title screen (viewed 21 May 2007). Submitted in fulfilment of the requirements for the degree of Doctor of Philosophy to the School of Public Health, Faculty of Medicine. Includes bibliographical references. Also available in print form.
Owen, Paul. "Body composition and function in chronic kidney disease". Thesis, University of Nottingham, 2013. http://eprints.nottingham.ac.uk/14576/.
Pełny tekst źródłaChakrabarti, Shubro. "Mechanisms of fibrosis in feline chronic kidney disease". Thesis, Royal Veterinary College (University of London), 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.572451.
Pełny tekst źródłaDarisipudi, Venkata Surya Narayana Murty. "Chemokines and cysteine proteases in diabetic kidney disease". Diss., Ludwig-Maximilians-Universität München, 2013. http://nbn-resolving.de/urn:nbn:de:bvb:19-173379.
Pełny tekst źródłaMontoya, Vicki. "Improving Chronic Kidney Disease Care with Group Visits". Doctoral diss., University of Central Florida, 2013. http://digital.library.ucf.edu/cdm/ref/collection/ETD/id/5676.
Pełny tekst źródłaPh.D.
Doctorate
Nursing
Nursing
Nursing
Afzal, Ali Reza. "Molecular studies of autosomal dominant polycystic kidney disease". Thesis, St George's, University of London, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.392478.
Pełny tekst źródłaLong, David Andrew. "Angiopoietin growth factors in models of kidney disease". Thesis, University College London (University of London), 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.401031.
Pełny tekst źródłaBrzoska, H. L. "Planar cell polarity in kidney development and disease". Thesis, University College London (University of London), 2017. http://discovery.ucl.ac.uk/1558749/.
Pełny tekst źródłaSimms, Roslyn Jane. "Zebrafish models of cystic kidney disease related ciliopathies". Thesis, University of Newcastle upon Tyne, 2013. http://hdl.handle.net/10443/2473.
Pełny tekst źródłaKhalaf, Fatimah. "Regulation of Renal Inflammation in Chronic Kidney Disease". University of Toledo Health Science Campus / OhioLINK, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=mco1588943852414778.
Pełny tekst źródłaBerezova, M. S., i S. A. Akentiev. "The effects of obesity on chronic kidney disease". Thesis, БДМУ, 2017. http://dspace.bsmu.edu.ua:8080/xmlui/handle/123456789/17110.
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